The main goal of this study was creating multifunctional nanoparticles based on rare-earth doped LaF 3 nanocrystals, which can be used as fluorescence thermal sensors operating over the 80-320 K temperature range including physiological temperature range (10-50 ∘ C). The Pr 3+ :LaF 3 ( Pr = 1%) microcrystalline powder and the Pr 3+ :LaF 3 ( Pr = 12%, 20%) nanoparticles were studied. It was proved that all the samples were capable of thermal sensing into the temperature range from 80 to 320 K. It was revealed that the mechanisms of temperature sensitivity for the microcrystalline powder and the nanoparticles are different. In the powder, the 3 P 1 and 3 P 0 states of Pr 3+ ion share their electronic populations according to the Boltzmann and thermalization of the 3 P 1 state takes place. In the nanoparticles, two temperature dependent mechanisms were suggested: energy migration within 3 P 0 state in the temperature range from 80 K to 200 K followed by quenching of 3 P 0 state by OH groups at higher temperatures. The values of the relative sensitivities for the Pr 3+ :LaF 3 ( Pr = 1%) microcrystalline powder and the Pr 3+ :LaF 3 ( Pr = 12%, 20%) nanoparticles into the physiological temperature range (at 45 ∘ C) were 1, 0.5, and 0.3% ∘ C −1 , respectively.

Localised extracellular interactions between nanoparticles and transmembrane signal receptors may well activate cancer cell growth. Herein, tiny LaF3 and PrF3 nanoparticles in DMEM+FBS suspensions stimulated tumour cell growth in three different human cell lines (A549, SW837 and MCF7). Size distribution of nanoparticles, activation of AKT and ERK signalling pathways and viability tests pointed to mechanical stimulation of ligand adhesion binding sites of integrins and EGFR via a synergistic action of an ensemble of tiny size nanoparticles (< 10 nm). While tiny size nanoparticles may be well associated with the activation of EGFR, integrin interplay with nanoparticles remains a multifaceted issue. A theoretical motif shows that, within the requisite pN force scale, each ligand adhesion binding site can be activated by a tiny size dielectric nanoparticle via electrical dipole interaction. The size of the active nanoparticle stayed specified by the amount of the surface charges on the ligand adhesion binding site and the nanoparticle, and also by the separating distance between them. The polar component of the electrical dipole force remained inversely proportional to the second power of nanoparticle’s size, evincing that only tiny size dielectric nanoparticles might stimulate cancer cell growth via electrical dipole interactions. The work contributes towards recognising different cytoskeletal stressing modes of cancer cells.Electronic supplementary materialThe online version of this article (10.1186/s11671-018-2775-z) contains supplementary material, which is available to authorized users.

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